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Another great guest post! – by Dr. Calvin Hwang, aka @helixcardinal – as well as the senior resident at Stanford/Kaiser EM program who updates the @StanfordEMRes residency twitter feed, provided an excellent case that illustrates a reason/indication to perform bedside ultrasound – especially the Echo/IVC and Aorta applications – illustrating why these applications are imperative to the RUSH protocol – along with good clinical judgement. Enjoy!

“Code 3 ringdown from EMS: 70 yo F coming in with 3 days of chest, back and abdominal pain, hypotensive with SBP in the 70s.

On arrival, patient is grimacing in pain, pale, diaphoretic. She is otherwise healthy with no past medical history. Just arrived from Thailand 1 week ago to visit her daughter and had been complaining of pain in her chest, back and abdomen. Went to a primary care physician where she was noted to be hypotensive and sent to the ED.

Initial vital signs: BP 73/30, HR 110, T37.0, RR 25

With the trusty bedside ultrasound, I immediately went to where I thought would be the diagnosis: ruptured AAA…..but…..

The abdominal aorta scan : I was shocked when I noticed it to be of normal caliber. Nevertheless, I worked my way up the abdomen to the subxiphoid view when I saw:

Though it was atypical for the patient to be hypotensive and tachycardic, the presence of a pericardial effusion without tamponade suggested aortic dissection to me. My attending got on the phone to prepare to transfer the patient while I contacted the radiologist to clear the CT scanner. Though I attempted to view the descending aorta and aortic outflow tract on a more focused echo in the brief interim through a parasternal approach, I was unable to obtain good windows. The IVC was plump and the rest of the FAST was negative. A quick Chest XR was done:

…..which did not show a wide mediastinum according to radiology. The patient was whisked away to the CT scanner and within 45 minutes of ED arrival, the diagnosis of a Stanford type A aortic dissection with pericardial effusion (but not tamponade) was confirmed. This would not have been possible without bedside ultrasound as I think most clinicians would have been falsely reassured by the normal CXR (widened mediastinum only present in 60% of aortic dissections1).

The patient was fluid resuscitated with crystalloid, her BP improved to 100/60 and HR came down to the 80s. While awaiting transport, I attempted to place an arterial line for close BP monitoring. However, approximately 60 minutes after ED arrival, the patient became progressively bradycardic and coded. My institution’s cardiothoracic surgeons were already at bedside and performed a sternotomy with pericardial window. Despite our efforts, we were never able to obtain return of spontaneous circulation and the patient was pronounced. These patients rarely make it to the ED due to how quickly they can decompensate, but if they do, quickening the diagnosis may help get them the intervention they need (clinical suspicion and appropriate use of bedside ultrasound is key), although a high mortality still exists.